Meta-analysis of the differentially expressed microRNA profiles in nasopharyngeal carcinoma

Luan, Junwen; Wang, Junfu; Su, Qinghong; Chen, Xuemei; Jiang, Guosheng; Xu, Xiaoqun

doi:10.18632/oncotarget.7013

Cited by 29 publications

(29 citation statements)

References 49 publications

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“…Several of the 24 significantly downregulated miRNAs identified in this study have previously been identified as tumor suppressor miRNAs in other malignancies, among others miR‐100‐5p, miR‐125b‐5p, miR‐127‐3p, miR‐370‐3p, miR‐335‐5p, and miR‐411‐5p (Gao et al ., ; He et al ., ; Jiang et al ., ; Li et al ., ; Luan et al ., ; Zhang et al ., ). Of these, miR‐100‐5p, miR‐127‐3p, and miR‐335‐5p have previously been identified as downregulated in OS studies analyzing 2–18 samples (Jones et al ., ; Maire et al ., ; Thayanithy et al ., ; Zhang et al ., ).…”

Section: Discussionmentioning

confidence: 99%

miRNA profiling identifies deregulated miRNAs associated with osteosarcoma development and time to metastasis in two large cohorts

et al. 2017

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Osteosarcoma (OS) is an aggressive bone tumor primarily affecting children and adolescents. The etiology of OS is not fully understood. Thus, there is a great need to obtain a better understanding of OS development and progression. Alterations in miRNA expression contribute to the required molecular alterations for neoplastic initiation and progression. This study is the first to investigate miRNA expression in OS in a large discovery and validation cohort comprising a total of 101 OS samples. We established the signature of altered miRNA expression in OS by profiling the expression level of 752 miRNAs in 23 OS samples using sensitive LNA‐enhanced qPCR assays. The identified miRNA expression changes were correlated with gene expression in the same samples. Furthermore, miRNA expression changes were validated in a second independent cohort consisting of 78 OS samples. Analysis of 752 miRNAs in the discovery cohort led to the identification of 33 deregulated miRNAs in OS. Twenty‐nine miRNAs were validated with statistical significance in the second cohort comprising 78 OS samples. miRNA/mRNA targets were determined, and 361 genes with an inverse expression of the target miRNA were identified. Both the miRNAs and the identified target genes were associated with multiple pathways related to cancer as well as bone cell biology, thereby correlating the deregulated miRNAs with OS tumorigenesis. An analysis of the prognostic value of the 29 miRNAs identified miR‐221/miR‐222 to be significantly associated with time to metastasis in both cohorts. This study contributes to a more profound understanding of OS tumorigenesis, by substantiating the importance of miRNA deregulation. We have identified and validated 29 deregulated miRNAs in the – to our knowledge – largest discovery and validation cohorts used so far for miRNA analyses in OS. Two of the miRNAs showed a promising potential as prognostic biomarkers for the aggressiveness of OS.

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Section: Discussionmentioning

confidence: 99%

miRNA profiling identifies deregulated miRNAs associated with osteosarcoma development and time to metastasis in two large cohorts

et al. 2017

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“…An increasing number of studies have attempted to examine tumor specific-miRNAs using the RRA method. Researchers used this method in multiple malignancies, including pancreatic, liver, renal, breast, colon, ovarian, bladder, and nasopharyngeal tract cancer [ 16 , 21 – 27 ]. Võsa U et al [ 6 ] first identified a panel of 15 aberrantly expressed miRNAs in lung cancer, including seven up-regulated miRNAs (miR-21, miR-210, miR-182, miR-31, miR-200b, miR-205 and miR-183) and eight down-regulated miRNAs (miR-126-3p, miR-30a, miR-30d, miR-486-5p, miR-451a, miR-126-5p, miR-143 and miR-145).…”

Section: Discussionmentioning

confidence: 99%

Identification of microRNAs as potential biomarkers for lung adenocarcinoma using integrating genomics analysis

et al. 2017

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Lung adenocarcinoma (LUAD) is the most common histological subtype of non-small cell lung cancer, but novel biomarkers for early diagnosis are lacking. Extensive effort has been exerted to identify miRNA biomarkers in LUAD. Unfortunately, high inter-lab variability and small sample sizes have produced inconsistent conclusions in this field. To resolve the above-mentioned limitations, we performed a comprehensive analysis based on LUAD miRNome profiling studies using the robust rank aggregation (RRA) method. Moreover, miRNA-gene interaction network, pathway enrichment analysis and Kaplan-Meier survival curves were used to investigate the clinical values and biological functions of the identified miRNAs. A total of six common differentially expressed miRNAs (DEMs) were identified in LUAD. An independent cohort further confirmed that four miRNAs (miR-21-5p, miR-210-3p, miR-182-5p and miR-183-5p) were up-regulated and two miRNAs (miR-126-3p and miR-218-5p) were down-regulated in LUAD tissues. Pathway enrichment analysis also suggested that the above-listed six DEMs may affect LUAD progression via the estrogen signaling pathway. Survival analysis based on the TCGA dataset revealed the potential prognostic values of six DEMs in patients with LUAD (P-value<0.01). In conclusion, we identified a panel of six miRNAs from LUAD using miRNome profiling studies. Our results provide evidence for the use of these six DEMs as novel diagnostic and prognostic biomarkers for LUAD patients.

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“…For example, Di et al observed that let-7d exerts both anti-oncogenic and oncogenic effects in osteosarcoma-derived 3AB-OS cancer stem cells [ 17 ]. In addition, let-7d reportedly directly targets HMGA2 [ 18 ], COL3A1, CCL7 and PBX3 [ 19 - 23 ], and thus suppresses tumor cell growth, migration, invasion, and metastasis. In this report, we describe our finding that elevated c-Myc is an unfavorable factor which promotes ovarian cancer pathogenesis, and that suppression of c-Myc by let-7d markedly sensitizes cancer cells to DFOG by downregulating the PI3K/AKT pathway.…”

Section: Introductionmentioning

confidence: 99%

Let-7d increases ovarian cancer cell sensitivity to a genistein analog by targeting c-Myc

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et al. 2017

Oncotarget

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c-Myc is a key oncogenic transcription factor that participates in tumor pathogenesis. In this study, we found that levels of c-Myc mRNA and protein were higher in early ovarian cancer tissues than normal ovary samples. Increased c-Myc levels correlated positively with clinical stage I (Ia+b/Ic) in ovarian cancer patients. Patients with higher nuclear c-Myc expression had shorter overall survival times than patients with low c-Myc expression. Knocking down c-Myc sensitized ovarian cancer cells to 7-difluoromethoxyl-5,4’-di-n-octylgenistein (DFOG), a novel synthetic genistein analogue that suppressed PI3K/AKT signaling in vitro and in vivo. Finally, c-Myc was confirmed to be a direct target of let-7d, and let-7d-induced suppression of c-Myc increased the DFOG-sensitivity of ovarian cancer cells. These results indicate that nuclear c-Myc expression is an unfavorable factor in early ovarian cancer, and that let-7d increases ovarian cancer cell sensitivity to DFOG by suppressing c-Myc and PI3K/AKT signaling.

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Meta-analysis of the differentially expressed microRNA profiles in nasopharyngeal carcinoma

Cited by 29 publications

References 49 publications

miRNA profiling identifies deregulated miRNAs associated with osteosarcoma development and time to metastasis in two large cohorts

miRNA profiling identifies deregulated miRNAs associated with osteosarcoma development and time to metastasis in two large cohorts

Identification of microRNAs as potential biomarkers for lung adenocarcinoma using integrating genomics analysis

Let-7d increases ovarian cancer cell sensitivity to a genistein analog by targeting c-Myc

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